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NURS 313R > Exam 3: Endocrine Disorders > Flashcards

Exam 3: Endocrine Disorders Flashcards

1
Q

Adrenal Gland

A

Upper portion of the kidney

Consists of medulla and cortex

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2
Q

The Adrenal Medulla is essential for

A

essential for response to stress

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3
Q

The Medulla secretes

A

secrete catecholamines, neurotransmitters (epinephrine, NE and dopamine)

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4
Q

Adrenal Cortex

A

outer part, secretes adrenal hormones called corticosteroids

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5
Q

What corticosteroids does the adrenal cortex secrete?

A

A. Glucocorticoid (cortisol)
B. Mineralocorticoids (aldosterone)
C. Androgen

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6
Q

Addison’s Disease

A

HYPOFUNCTION OF ADRENAL CORTEX

  • adrenocortical insufficiency, all three classes of adrenal corticosteroids are reduced
  • autoimmune response
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7
Q

Causes of Addison’s Disease include

A
  • Autoimmune (your own antibodies destroy your own adrenal cortex leading to a decrease in hormone production)
  • Fungal infections
  • AIDS
  • Cancer
  • Iatrogenic (anticoagulant, antineoplasm)
  • Adrenalectomy
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8
Q

Clinical Manifestations of Addison’s Disease does not become evident until

A

until 90% of the adrenal cortex is destroyed

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9
Q

Primary clinical manifestations of Addison’s Disease include

A
  • progressive weakness
  • fatigue
  • wt. loss
  • anorexia
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10
Q

Other clinical manifestations of Addison’s Disease include

A
  • skin hyperpigmentation (sun exposed areas) joint, pressure points palmar crease.
  • Hypotension
  • Hyponatremia (d/t opposite effect of mineralcorticoids)
  • Hyperkalemia
  • Nausea, vomiting, diarrhea (caused by hyperkalemia - increases peristaltic movement in GI)
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11
Q

Complications of Addison’s Disease include

A

Addisonian Crisis

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12
Q

Addisonian Crisis

A

Acute adrenal insufficiency triggered by stress or sudden withdrawal fo corticosteroid therapy

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13
Q

Symptoms of Addisonian Crisis include

A
  • Hypotension (postural but from low fluid volume)
  • Tachycardia (lack of aldosterone)
  • Dehydration (d/t diarrhea from hyperkalemia)
  • Hyponatremia (lack of aldosterone)
  • Hyperkalemia
  • Hypoglycemia (no production of glucocorticoids)
  • Fever
  • Weakness
  • Confusion (d/t hypoglycemia - brain needs glucose)
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14
Q

Collaborative Care for Addison’s Disease includes

A
  • daily glucocorticoid replacement (2/3 on awakening in AM 1/3 in late PM)
  • shock management
  • fluid replacement (large volume of 0.9% saline solution)
  • mineralcorticoids – once daily in AM
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15
Q

Acute Intervention of patients with Addison’s Disease

A
  • vital signs, fluid volume deficit / electrolytes, assess every 30 min to 4 hours for 1st 24 hours
  • daily wt.
  • corticosteroid administration
  • keep follow up appointment
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16
Q

A patient with Addison’s disease should be protected against

A

protect against exposure to infection, noise, light and extreme temperature (could lead to addisonian crisis)

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17
Q

Ambulatory Care for Patients with Addison’s Disease

A
  • carry a medic alert
  • fluid replacement
  • carry emergency kit (100mg IM hydrocortisone , syringe**)
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18
Q

Patient Teaching for Patient’s with Addison’s Disease

A
  • Teach the importance of life long replacement therapy
  • Teach additional exogenous corticosteroid adjustment secondary to stress

a. double dose when minor stress occurs
b. triple dose for major stress

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19
Q

Pheocromocytoma

A
  • rare condition characterized by tumor of the adrenal medulla that produce excessive catecholamines (epinephrine, norepinephrine)
  • results in severe hypertension
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20
Q

Clinical Manifestatons of Pheocromocytoma

A
  • severe episodes of hypertension
    * severe pounding headache*
    * palpitation
    * profuse sweating*
  • anxiety
  • tachycardia*
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21
Q

Nursing Therapeutics/Collaborative Management for Pheocromocytoma

A
  • surgical removal of tumor
  • pre op sympathetic blocking agent (eg. Minipress, cardura) to decrease symptoms of catecholamine excess monitor for orthostatic hypotension
  • metyrosine – adm. to diminish catecholamine production if surgery is not an option, may cause orthostatic hypotension
  • monitor triad symptoms
  • emotional support
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22
Q

Disorders Associated with ADH Secretions

A
  • SIADH

- Diabetes Insipidus

23
Q

ADH

A

Produced in hypothalamus and transported/stored in posterior pituitary gland.
Causes body to retain water and as a result there will be a decrease in urine output.

24
Q

SIADH

A

Syndrome of inappropriate ADH.

Overproduction of ADH

25
Q

Diabetes Insipidus

A

Underproduction or undersecretion of ADH

26
Q

SIADH occurs when

A

ADH is release despite normal or low plasma osmolarity

27
Q

SIADH is characterized by

A
  • Fluid Retention
  • Serum Hypoosmolarity
  • Dilutional Hyponatremia
  • Hypocholermia
  • Concentrated urine in the presence of normal or increased intravascular volume and normal renal function
28
Q

Causes of SIADH include

A
  • malignant tumor (can produce and store, and release ADH)
  • CNS Disorder (CVA, Head Injury)
  • Drug Therapy (tegretol, diabenese, opoids, thiazides, tricyclic antidepressant
29
Q

Clinical Manifestations of SIADH

A

• Extra cellular volume expands
• Plama osmoality declines
• Glomerular filtration rate increase (d/t high volume of fluid)
• Dilutional hyponatremia
• Low urine output, increase body wt.
• Vomiting, abdominal cramps, muscle twitching, seizure (d/t low sodium levels)
• Cerebral edema, lethargy, anorexia, confusion (d/t low sodium levels and water retention)
• Headache, seizure and coma (d/t cerebral edema)
NO PERIPHERAL EDEMA

30
Q

Collaborative Care Goal for SIADH

A

Restore normal fluid volume osmolarity

31
Q

Collaborative Care for SIADH include

A
  • Restrict fluid intake to 800-1000 ml/day
  • IV hypertonic solution , administer very slowly via pump
  • Lasix to promote diuresis
32
Q

Nursing Therapeutics for SIADH

A
  • Assess v/s, I&O, daily wt.,LOC, s/s of hyponatremia, cardiac assessment
  • Restrict fluid intake no more than 1000ml/day include meds
  • Position of bed flat or no more than 10 degree elevation
  • Seizure precaution
  • Supplement diet with sodium
33
Q

What should the nurse teach a patient with SIADH to do to decrease thirst?

A

Suck on hard candy to decrease thirst

34
Q

Diabetes Insipidus

A
  • Is a group of conditions associated with a deficiency of production or secretion of ADH or decrease renal response to ADH.
  • lead to increase renal output and increase plasma osmolality
35
Q

What are clinical manifestations of diabetes insipidus?

A 
•	polydipsia
•	polyuria (5-20 L/day)
•	very low specific gravity
•	elevated osmolality (due to pure water loss)
SYMPTOMS D/T SEVERE DEHYDRATION:
•	nocturia, weakness (d/t large urine output during night time hours, weakness d/t dehydration and poor oxygen perfusion d/t Hypovolemia)
•	wt.loss, constipation
•	poor skin turgor
•	hypotension
•	tachycardia
•	shock
36
Q

Collaborative Care Goal for Patients with Diabetes Insipidus

A

Maintain fluid and electrolyte balance

37
Q

Collaborative Care for Diabetes Insipidus

A
  • Hormonal Replacement
  • Hypotonic Saline Administration IV or D5W (monitor glucose levels because hyperglycemia and glycosuria can lead to osmotic diuresis and increase fluid volume deficit)
  • Drugs
  • Sodium intake no more than 3 g/day
38
Q

What drugs are used to treat diabetes insipidus?

A 
Pitressin
Diapid
Indocin
Tegretol
Diabenese
39
Q

Nursing Therapeutics for Patients with Diabetes Insipidus

A
  • adequate p.o and IV hydration
  • monitor urine for glucose if IVF glucose due to osmotic diuretic
  • I & O, wt monitoring
40
Q

Glucocorticoids

A

Regulates metabolism
Increases blood glucose levels
Critical in physiologic stress response.

41
Q

Mineralcorticoids

A

Regulates Na and K balance

42
Q

Androgens

A

Contribute to the growth and development of both genders and sexual activity in adult women.

43
Q

Cushing’s Syndrome

A

Clinical abnormalities caused by EXCESS CORTICOSTEROIDS -> particularly glucocorticoids

44
Q

What can cause Cushing’s?

A
  1. Iatrogenic administration of exogenous corticosteroids (prednisone)
  2. ACTH-secreting pituitary adenoma: stimulates glucocorticoids -> increase blood sugar
  3. Adrenal tumors and ectopic ACTH production by tumors outside of the hypothalamic-pituitary adrenal axis -> excess release of glucocorticoids
45
Q

Clinical Manifestations of Cushing’s Disease

A
  1. Weight gain; BUFFALO HUMP in neck (d/t accumulation of adipose tissue in the trunk, face and cervical spine area)
  2. HYPERGLYCEMIA (d/t glucose intolerance and increased gluconeogenesis by the liver)
  3. Muscle wasting (weakness of extremities)
  4. Osteoporosis/pathological fracture (d/t loss of protein matrix in bone)
  5. Weak/thin Skin (d/t loss of collagen)
  6. MOON FACE (d/t increase in mineralcorticoids -> sodium and water retention)
  7. Mood disturbances
  8. Delayed wound healing
  9. Thinning hair
  10. Hypertension (sodium and water retention)
  11. Severe Acne
  12. Menstrual disorders, hirsutism in women
  13. Feminization, gynecomastia and impotence in men
46
Q

The clinical presentation is the first indication of Cushing syndrome with particular importance on

A

(1) centripetal (truncal) obesity or generalized obesity;
(2) “moon facies” (fullness of the face) with facial plethora;
(3) purplish red striae (usually depressed below the skin surface) on the abdomen, breast, or buttocks;
(4) hirsutism in women;
(5) menstrual disorders in women;
(6) hypertension;
(7) unexplained hypokalemia

47
Q

What can indicate Cushing;s Syndrome?

A
  1. 24 hour urine collection: >80-120 mcg
  2. Dexamethason Suppression Test
  3. MRI & CT of adrenal and pituitary gland
  4. Increased plasma ACTH = Cushing’s disease
  5. Decreased or normal ACTH = Cushing’s syndrome
48
Q

Collaborative Care for Cushing’s Disease

A
  • Primary goal is to normalize hormone secretion.
  • Surgical removal of tumor (adrenalectomy)
  • Drug therapy prior to surgery
49
Q

Drug therapy prior to surgery for Cushing’s include

A

Mitotane and Ketoconazole

50
Q

Mitotane

A

The inhibition of adrenal Function -> suppresses cortisol production and decrease plasma and urine corticosteroid levels.
Needed before surgery because surgery is a stressful event that increases cortisol production.

51
Q

Ketoconazole

A

Blocks key enzymes in the body for essential production of corticosteroids.

52
Q

Nursing Therapeutics for Cushing’s

A
  • Monitor for S&S of thromboembolic events
  • Emotional support -> body image disturbances
  • Control of HTN, hyperglycemia and hypokalemia
53
Q

Ambulatory home care for Cushing’s

A
  • Stress may produce or precipitate acute adrenal insufficiency.
  • Lifetime replacement therapy
  • Wear medical alert bracelet
  • Avoid exposure to extremes of temperature, infections and emotional disturbances
54
Q

If pheocromocytoma is left untreated,

A

-Hypertensive Encephalopathy
-DM
-Cardiomyopathy
-Death
Can occur.

NURS 313R (18 decks)

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